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http://purl.uniprot.org/citations/12810606http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12810606http://www.w3.org/2000/01/rdf-schema#comment"

Background

Insulin resistance is associated with atherosclerosis, but its mechanism is unknown. It has been reported that insulin receptor substrate (IRS)-1 deficient (IRS-1-/-) mice showed insulin resistance without type 2 diabetes, whereas the IRS-2 deficient (IRS-2-/-) mice showed insulin resistance with type 2 diabetes.

Methods and results

We investigated neointima formation in the IRS-1-/- and IRS-2-/- mice at 8 and 20 weeks. The IRS-2-/-mice showed much greater neointima formation than the IRS-1-/- and wild-type mice at 8 weeks. At 20 weeks, the IRS-2-/-mice had greater neointima formation than the IRS-1-/-mice, which showed more enhanced neointima formation than the wild-type mice. The IRS-1-/- and IRS-2-/-mice had dyslipidemia, hypertension, and insulin resistance. The IRS-2-/-mice had more metabolic abnormalities than the IRS-1-/-mice at 8 and 20 weeks. IRS-2 expression was detected, but IRS-1 expression was not detected in the vessels.

Conclusions

The neointima formation in the IRS-1-/- and IRS-2-/-mice appears to be related to abnormalities induced by the altered metabolic milieu in insulin-resistant states. Moreover, because neointima formation was much greater in the IRS-2-/- mice than in the IRS-1-/-mice at 8 and 20 weeks, it is suggested that a lack of IRS-2 renders the vasculature more susceptible to injury in the abnormal metabolic milieu, and IRS-2 may have a protective effect on neointima formation. We conclude that IRS-2 is protective and retards the development of neointima formation in insulin-resistant states."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.org/dc/terms/identifier"doi:10.1161/01.cir.0000070937.52035.25"xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Kobayashi T."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Aizawa S."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Yamaguchi T."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Kadowaki T."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Kubota T."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Suzuki R."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Kamata K."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Kubota N."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Nagai R."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Terauchi Y."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Tobe K."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Moroi M."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/author"Namiki A."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/date"2003"xsd:gYear
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/name"Circulation"xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/pages"3073-3080"xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/title"Lack of insulin receptor substrate-2 causes progressive neointima formation in response to vessel injury."xsd:string
http://purl.uniprot.org/citations/12810606http://purl.uniprot.org/core/volume"107"xsd:string
http://purl.uniprot.org/citations/12810606http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12810606
http://purl.uniprot.org/citations/12810606http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12810606
http://purl.uniprot.org/uniprot/#_P35569-mappedCitation-12810606http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12810606
http://purl.uniprot.org/uniprot/#_O88970-mappedCitation-12810606http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12810606
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